Hi dude, sorry for delay.
Long mail; get tea  :  )

This is in reference to burnout, where levels of neurochemicals and number of functional receptors tend to increase up to a critical mass where the burnout occurs, and then plummet below 'normal' levels. This pattern, where (for example) elevated cortisol followed by big reductions in cortisol, is indicative of burnout. A regular case of excess of anything will cause temporary down-regulation of receptors, but in burnout there is more widespread down-regulation which may if not adjusted be permanent. In some cases certain areas are initially up-regulated at the expense of others.

From the original paper:
Interestingly, in the amygdala, stress seems to lead to an increase in neurotrophic factors such as BDNF, and to enhance dendritic outgrowth. In the functional and anatomical projection areas of the amygdala, the stress-related glutamatergic excess is, on the other hand, reported to lead to reduced BDNF and shrinkage of dendrites (Arendt et al. 2012; Boyle 2013). These degenerative events are particularly pronounced in the mPFC (Roozendaal et al. 2004; Brown et al. 2005; Radley et al. 2008; Arnsten 2009; Leuner and Shors 2012).

This is of interest because the mPFC exerts a strong negative control over stress pathways. GABAergic signals from the mPFC to the amygdala lead to a repression of the HPA axis. This provides a basis for one possible scenario for the present condition, in which stress-mediated neurotoxic damage to the mPFC, due to high glutamate, cortisol, or the combination of both (see Magarinos and McEwen 1995), has led to impaired prefrontal inhibition of the amygdala (Roozendaal et al. 2004). This would then have provided a context for a vicious circle with a further enhancement of amygdala excitation and subsequent changes along the networks connected to the amygdala (the mPFC, the basal ganglia, the hippocampus, and the insular, anterior cingulate, and orbitofrontal cortices).

The presently reported findings among subjects suffering from occupational stress fit into this model, with the increase in amygdala volume and reduction in caudate volume, the thinning of the mPFC, and the more pronounced cortico-cortical covariation between the mPFC and insular cortex (Wang et al. 2007; Liston et al. 2009; Goldstein et al. 2010). It is also compatible with the notion that both the putamen and caudate receive powerful glutamatergic input from the amygdala (McEwen 2000b) and are susceptible to excitotoxicity (Chen et al. 1995; Bernal et al. 2000). This strengthens reiterating the hypothesis presented in our initial stress-related publication (Jovanovic et al. 2011) that repeated stress stimuli could cause excitotoxic, apoptotic, and/or intermediate forms of neuronal death (Bengzon et al. 1997) with atrophy in humans.


Here is one of the original papers:
http://cercor.oxfordjournals.org/conten … ull#ref-12


There has been more recent discovery in the field of synaptic plasticity which is relevant to the above in context of altered BDNF levels:

DOI: 10.1038/nature19766/10.1038/nature19784 Stephen C. Harward et al. Autocrine BDNF–TrkB signalling within a single dendritic spine, Nature (2016). DOI: 10.1038/nature19766

Nathan G. Hedrick et al. Rho GTPase complementation underlies BDNF-dependent homo- and heterosynaptic plasticity, Nature (2016). DOI: 10.1038/nature19784 

"Two new studies uncover key players responsible for learning and memory formation" October 3, 2016 http://medicalxpress.com/news/2016-10-uncover-key-players-responsible-memory.html

Best,
AR

Yeh this is the fun with brains  :  )
Researchers narrow down an area that appears to be specializing in one or two data types, and think, great, we'll call this part 'the amygdala' (or whatever). Then you go look at what the amygdala is doing, and you find half a dozen different compartments all doing different things, or different bits of the same task... so you select one and think okay, we'll call this part the 'rostral amygdala', and you look at what it's doing, and you find... oh yeh, another little batch of individual parts in there, doing different things...
...I guess we already know that this sort of thing doesn't stop at the atomic level  :  )

Tea in Wonderland:
...“Take some more tea," the March Hare said to Alice, very earnestly.
"I've had nothing yet," Alice replied in an offended tone, "so I can't take more."
"You mean you can't take less," said the Hatter: "it's very easy to take more than nothing."

Best,
AR

Tea issues can be solved by DIY:

http://www.camforest.com/category_s/53.htm

(and a whole host of other benefis from gardening activities)
Best,
AR